No abstract available.
Embryo Transfer* ; Embryonic Structures* ; Fertilization in Vitro* ; Pregnancy*

The purposes of this study were to evaluate the effects of insulin-like growth factor (IGF)s in peritoneal fluid (PF) from patients with and without endometriosis on the proliferation of endometrial stromal cells and to investigate the effects of type I IGF receptor antibody on the response of endometrial stromal cells to PF from patients with endometriosis. IGFs in PF from patients with endometriosis (n=14) and without endometriosis (n=10) were measured by immunoradiometric assay and PF samples were divided into low IGF-I PF group (less than 85 ng/ml) and high IGF-I PF group (more than 85 ng/ml). Endometrial stromal cells from patients without endometriosis were cultured in serum free media in the presence or absence of 1% PF and thymidine incorporation test were used to evaluate the proliferation of endometrial stromal cells. Also cultures were incubated with type I IGF receptor monoclonal antibody (alpha IR3) before adding PF. PF from patients with endometriosis and without endometriosis increased thymidine incorporation in endometrial stromal cells. In patients with endometriosis, high IGF-I PF group had high IGF-II levels and resulted in higher thymidine incorporation than low IGF-I PE and low IGF-I PF group was noted in patients without endometriosis. There was not a significant correlation between increase in thymidine incorporation and IGF-I levels in PF from patients without endometriosis but in PF from patients with endometriosis. Preincubation with alphaIR3 significantly inhibited the mitogenic response of endometrial stromal cells to PF. Our data indicate that IGF-I in PF may be involved in the growth of ectopic endometrium in patients with endometriosis.
Ascitic Fluid* ; Culture Media, Serum-Free ; Endometriosis* ; Endometrium ; Female ; Humans ; Immunoradiometric Assay ; Insulin-Like Growth Factor I ; Insulin-Like Growth Factor II ; Stromal Cells* ; Thymidine

BACKGROUND: Sex steroid hormones are believed to play an important role in the genesis and growth of uterine myoma. Several studies suggest a possible role of insulin-like growth factor(IGF) as a mediator of estradiol in uterine myama. We have recently demonstrated that some IGF binding proteins(IGFRPs) messenger ribonucleic acid(mRNA) expressions in myoma are dependent on the in vivo esttogen status. The purposes of this study are to evaluate the in vitro effects of sex steroid hormones including estrogen on the IGFBPs gene expression in tissues from uterine myoma and adjacent normal myometrium. METHODS: Tissues from myoma and adjacent normal myometrium of patients with uterine myoma during early proliferative phase of menstrual cycle were cultured in the absence(control) and presence of 17b-estradiol(10M/L) or/and progesterone(10M/L) for 3 days. The IGFBPs mRNA expressions in these explants were analyzed by Nothern blot using specific human complementary deoxyribonucleic acid(cDNA) probes. RESULTS: The addition of 17b-estradiol, progesterone alone and in combination to conditioned media of explants from myoma and adjacent normal myornetrium did not result in any changes in the expression of IGFBP-2, IGFBP-4, IGFBP-5, and IGFBP-6 mRNA. With progesterone addtion, lGFBP-3 rnRNA expression was significantly reduced in myoma explant but not in adjacent ncemal myometrium explant. There was no significant change in the IGFBP-3 mRNA expression with 17b-estradiol and with the combination of both 17b-estradiol and progesterone. CONCLUSION: 17b-estradiol does not affect IGFBPs gene expression in the myoma and adjacent normal myometrium explant regardless of the presence of progesterone in vitro. However progesterone alone induces a decrease in IGFBP-3 synthesis in myoma explant.
Animals ; Culture Media, Conditioned ; Estradiol ; Estrogens ; Female ; Gene Expression ; Gonadal Steroid Hormones ; Humans* ; Insulin-Like Growth Factor Binding Protein 2 ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Protein 4 ; Insulin-Like Growth Factor Binding Protein 5 ; Insulin-Like Growth Factor Binding Protein 6 ; Insulin-Like Growth Factor Binding Proteins ; Leiomyoma* ; Menstrual Cycle ; Mice ; Myoma ; Myometrium* ; Progesterone ; RNA, Messenger*

Leiomyoma is benign tumor, which usually occurs at the smooth muscle of gastrointestinal tract and uterus but leiomyoma on the penis is very. rare neoplasm. We experienced a case of leiomyoma on the penis in a 17 year old man, so we report this case with review of literatures.
Adolescent ; Gastrointestinal Tract ; Humans ; Leiomyoma* ; Male ; Muscle, Smooth ; Penile Neoplasms ; Penis* ; Uterus

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and t,he incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*

BACKGROUND: PUVA has been used effectively in the treat,ment of vitiligo, but the mechanism by which PUVA stimulat.es melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and t,he incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes* ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo*

PURPOSES: To evaluate the effect of hormone replacement therapy(HRT) on serum insulin-like growth factors(IGFs) levels and to investigate if changes in serum IGFs reflect changes in BMD after HRT in postmenopausal women. MATERIAL & METHODS: IGF-I and IGF-II were measured by radioimmunoassay after Bio-spin P-10 seperation in sera obtained every 3 months from postmenopausal women who was taking premarin alone (premarin group; n=17) or premarin-medroxyprogesterone acetate(MPA group; n=42) for 1 year. Also, bone mineral density(BMD) were determined before and 1 year after HRT by dual energy X-ray absorptiometry(DEXA). All statistics were performed by Paired t-test, student's t-test, repeated measures ANOVA test, Pearson's coefficient. RESULTS: HRT increased BMD of the lumbar spine and proximal femur in both premarin group and MPA group, but any difference in degreee of increase in BMD was not noted between premarin group and MPA group. Compared with pretreatment levels, serum IGF-I levels decreased at 3, 6 and 12 months after therapy only in latter group whereas serum IGF-II levels increased at 6 and 12 months after HRT in both groups. Changes in serum IGF-I and IGF-II levels during therapy did not show any difference by the bone response to HRT. Changes in serum IGF-II levels after HRT did not correlated with the 1 year changes in BMD at any skeletal sites studied, but changes in serum IGF-I levels from pretreatment to 6 months after HRT was negatively correlated with change in BMD of Ward's triangle. CONCLUSION: HRT influences serum IGF levels in postmenopausal women and changes in serum IGF-I levels may predict the changes in BMD of Ward's triangle after HRT.
Bone Density* ; Estrogens, Conjugated (USP) ; Female ; Femur ; Hormone Replacement Therapy* ; Humans ; Insulin-Like Growth Factor I ; Insulin-Like Growth Factor II ; Postmenopause ; Radioimmunoassay ; Spine

Augmentin is a formulation of amoxycillin trihydrate and potassium clavulanate, a fused beta-lactam molecule produced by the fermentation of straptomyces clavuligerus. Most clinically important resistance is due to the production by bacteria of antibiotic destroying enzymes. In the case of penicillins and cephalospolins these enzymes are termed beta-lactamse as they destroy the beta-lactam ring of these antibiotics completely inactivating them. The presence of clavulanic acid extends the spectrum of amoxycillin to include beta-lactamse producing strains of common pathogens such as Staphylococcus, H influenza, E. coli, Neisseria spp, Proteus spp, Salmonella and Shigella. On clinical study of Augmenting in the field of Genitourinary tract infection cases. We selected randomly 30 patients, 20 males and 10 females, age from 21 to 71, in the period from October, 1985 to February, 1986. Among the total 30 patients, 15 were uncomplicated urinary tract infection and 15 were complicated urinary tract infection. Of the 15 patients with uncomplicated urinary tract infection, 14 patients had not bacteriuria after therapy and 1 patient was not changed. The clinical efficacy rate was 93.4%. Of the 4 patients with persistent infection, 2 patients had resistant P. aeruginosa, and 2 patients had S marcescens persistantly. The clinical efficacy rate was 73.4%. In 2 cases, mild diarrhea was developed, but medication was not stopped. The liver and renal function were normal range before and after treatment.
Amoxicillin ; Amoxicillin-Potassium Clavulanate Combination* ; Anti-Bacterial Agents ; Bacteria ; Bacteriuria ; beta-Lactams ; Clavulanic Acid ; Diarrhea ; Female ; Fermentation ; Humans ; Influenza, Human ; Liver ; Male ; Neisseria ; Penicillins ; Proteus ; Reference Values ; Salmonella ; Shigella ; Staphylococcus ; Urinary Tract Infections

No abstract available.
Acanthosis Nigricans* ; Growth Hormone*

PURPOSE: This study was to confirm the effect of acupressure on the emesis control and the weight change among pediatric cancer patients receiving anti-cancer chemotherapy. METHOD: Forty pediatric cancer patients, receiving the induction stage of chemotherapy with MTX and vincristine, were divided into control(n=20) and the intervention group(n=20). Both groups received regular anti-emesis medication, but the intervention group was added acupressure maneuver for 5 minutes on P6 point for 3 times a day for 5days: before chemotherapy, lunch and dinner by investigator during the hospitalization and by mother at home. The instruments for this study were Rhode's(1986) Index of nausea, vomiting and retching(INVR), Cas electric scale and pamphlet developed by researcher. RESULT: Significant differences in the degree of nausea and vomiting were observed between the control and the intervention group as measured by INVR(t=4.73; p=.01). Repeated measures ANOVA also shows that the group effect was significant(F=22.39, P=.01) as was the time effect(F=380.35, P=.01). The group by time interaction was also significant(F=5.27, P=.01). Acupressure maneuver was apparently effective in reducing the degree of chemotherapy-induced nausea and vomiting. There were also statistically significant weight loss noted in the control group than the intervention group(t=5.42, p=.01). CONCLUSION: Acupressure on P6 point shows an effective adjunct maneuver in reducing the degree of nausea and vomiting and conserving the weight in pediatric cancer patients. Therefore, it is proposed that acupressure should be applied as supportive nursing intervention strategies to relieve chemotherapy induced nausea and vomiting and to prevent weight loss in pediatric cancer patients.
Acupressure* ; Drug Therapy* ; Hospitalization ; Humans ; Lunch ; Meals ; Mothers ; Nausea ; Nursing ; Pamphlets ; Research Personnel ; Vincristine ; Vomiting ; Weight Loss ; Child Health